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Biomedical subjects

A Corti

Publications and source records attributed to A Corti.

At least 127 records · Page 7Linked to original sources
PubMed1985

Solid-phase enzyme-receptor assay (SPERA): a competitive-binding assay for glycopeptide antibiotics of the vancomycin class.

A solid-phase enzyme-receptor assay (SPERA) has been developed for glycopeptide antibiotics of the vancomycin class such as teicoplanin, vancomycin, ristocetin, avoparcin, actaplanin, A-47934, A-41030, and A-35512-B. The assay exploits the mechanism of most action of these antibiotics, which is based on their interaction with acyl-D-alanyl-D-alanine, a constituent of the walls of most growing bacterial cells. The antibiotics and enzyme-labeled teicoplanin compete for a synthetic analog of the biological receptor, albumin-epsilon-aminocaproyl-D-alanyl-D-alanine. The various antibiotics produced different competition curves, 50% displacement being obtained with antibiotic concentrations ranging from 0.04 to 4 mg/L, vancomycin and actaplanin being the weakest and strongest competitors, respectively. For teicoplanin in human serum the intra-assay CV was 7.2%, the interassay CV was 11.2%, and the analytical recovery 94%. Teicoplanin concentrations obtained by SPERA (chi) correlated well with those obtained by microbiological assay (y): y = 1.03 chi + 0.053 (r = 0.943; n = 60). We conclude that SPERA is a powerful tool for identification and quantitative detection of glycopeptide antibiotics, even in complex media.

Anti-Bacterial Agents↗
PubMed1985

Binding of the glycopeptide antibiotic teicoplanin to D-alanyl-D-alanine-agarose: the effect of micellar aggregates.

Teicoplanin, as well as the other antibiotics of the vancomycin group, was shown to bind specifically to D-alanyl-D-alanine-agarose (D-Ala-D-Ala-AGA) (A. Corti and G. Cassani, Appl. Biochem. Biotechnol. 11, 101-110 (1985)). This finding is extended, showing that the binding is as a function of concentration and physical form of the antibiotic in solution, i.e., monomers or micellar aggregates. At concentrations below the critical micelle concentration (CMC) teicoplanin binds with an affinity and a capacity similar to the other antibiotics of the same group such as vancomycin and ristocetin A. At concentrations above the CMC three times more teicoplanin is bound to D-Ala-D-Ala-AGA than the other two antibiotics. Equilibrium binding experiments carried out at different pHs with teicoplanin in the monomeric or micellar form indicate that the excess binding of teicoplanin occurs in the presence of micelles. Elaboration of binding data according to Scatchard indicates that the maximum binding capacity of the resin is increased 3.6 times when teicoplanin is in the micellar form. On the contrary, the apparent binding affinity is lower.

Chemical Phenomena↗
PubMed1984

Monoclonal antibodies to human urokinase identify the single-chain pro-urokinase precursor.

Monoclonal antibodies have been obtained that recognize either the A or B chain of human urinary urokinase. These antibodies identify human urokinase-producing cells and the product of urokinase mRNA. Anti-urokinase monoclonal antibodies precipitate an approximately equal to 54,000-dalton protein synthesized in vitro in a rabbit reticulocyte cell-free system. This pro-urokinase appears to be the precursor of both A and B chains of human urinary urokinase. Urokinase mRNA in human kidney constitutes only 0.1% or less of total poly(A)+ RNA.

Animals↗
PubMed1984

Teicoplanin, a new antibiotic from Actinoplanes teichomyceticus nov. sp.

Teicoplanin, a new glycopeptide antibiotic belonging to the same family as vancomycin, inhibits cell wall synthesis in Bacillus subtilis; the inhibition is accompanied by an intracellular accumulation of UDP-N-acetyl-muramyl-pentapeptide. A cell-free system from Bacillus stearothermophilus, capable of synthesizing peptidoglycan, is 50% inhibited by teicoplanin at 40 micrograms/ml and 100% inhibited at 100 micrograms/ml; suppression of peptidoglycan synthesis is accompanied by parallel accumulation of the lipid intermediate. Teicoplanin binds to cell walls and forms a complex with N,N'-diacetyl-L-lysyl-D-alanyl-D-alanine. The association constant of this complex is 2.56 X 10(6) liters mol-1, calculated by spectrophotometric titration. The mechanism of action of teicoplanin is discussed in comparison with those of other inhibitors of cell wall biosynthesis, namely, vancomycin, ristocetin, and gardimycin.

Acetylglucosamine↗
PubMed1983

Peptide chain initiation and analysis of in vitro translation products in rat heart undergoing hypertrophic growth.

The cytosol fraction of rat heart contains an initiation factor-like protein component that behaves like the eukaryotic factor (eIF-2) in binding [35S]-Met-tRNAf in the presence of GTP. The ternary initiator complex thus formed is able to bind to heart ribosomes. In the left ventricle of rat heart undergoing hypertrophic growth upon constriction of the descending aorta, the [35S]-Met-tRNAf binding activity of the cytosol protein(s) gradually increases after the operation from 40%, at 48 h, to 90%, at 10 days; slightly lower activation is seen in the [35S]-Met-tRNAf binding to ribosomes. Polysomal RNA is extracted from sham operated and hypertrophic rat hearts and translated in a reticulocyte cell free system. The translation products are analyzed by sodium dodecyl sulphate-polyacrylamide gel electrophoresis: no clearcut qualitative difference is observed in the pattern obtained from sham operated and hypertrophic animals.

Animals↗
PubMed1979

The decarboxylation of S-adenosylmethionine by detergent-treated extracts of rat liver.

1. The production of (14)CO(2) from S-adenosyl[carboxyl-(14)C]methionine by rat liver extracts was investigated. It was found that, in addition to the well-known cytosolic putrescine-activated S-adenosylmethionine decarboxylase, an activity carrying out the production of (14)CO(2) could be extracted from a latent, particulate or membrane-bound form by treatment with buffer containing 1% (v/v) Triton X-100 [confirming the report of Sturman (1976) Biochim. Biophys. Acta428, 56-69]. 2. The formation of (14)CO(2) by such detergent-solubilized extracts differed from that by cytosolic S-adenosylmethionine decarboxylase in a number of ways. The reaction by the solubilized extracts did not require putrescine and was not directly proportional to time of incubation or the amount of protein added. Instead, activity a showed a distinct lag period and was much greater when high concentrations of the extracts were used. The cytosolic S-adenosylmethionine decarboxylase was activated by putrescine, showed strict proportionality to protein added and the reaction proceeded at a constant rate. Cytosolic activity was not inhibited by homoserine or by S-adenosylhomocysteine, whereas the Triton-solubilized activity was strongly inhibited. 3. By using an acetone precipitate of Triton-treated homogenates as a source of the activity, it was found that decarboxylated S-adenosylmethionine was not present among the products of the reaction, although 5'-methylthioadenosine and 5-methylthioribose were found. Such extracts were able to produce (14)CO(2) when incubated with [U-(14)C]-homoserine, and (14)CO(2) production was greater when S-adenosyl[carboxyl-(14)C]methionine that had been degraded by heating at pH6 at 100 degrees C for 30min (a procedure known to produce mainly 5'-methylthioadenosine and homoserine lactone) was used as a substrate than when S-adenosyl[carboxyl-(14)C]methionine was used. 4. These results indicate that the Triton-solubilized activity is not a real S-adenosylmethionine decarboxylase, but that (14)CO(2) is produced via a series of reactions involving degradation of the S-adenosyl-[carboxyl-(14)C]methionine. It is probable that this degradation can occur via several pathways. Our results would suggest that part of the reaction occurs via the production of S-adenosylhomocysteine, which can then be converted into 2-oxobutyrate via the transsulphuration pathway, and that part occurs via the production of homoserine by an enzyme converting S-adenosylmethionine into 5'-methylthioadenosine and homoserine lactone.

Adenosylmethionine Decarboxylase↗
PubMed1979

[Separate extraction of 2 fractions of Mn++-dependent poly-A polymerase activity in liver cell nuclei of rats].

Part of the Mn++-dependent poly(A) polymerase activity of rat liver nuclei leaks out of the organelles when they are suspended in isotonic sucrose. With 0.5 ml/g fresh tissue of medium or more no increase in enzyme leaking out occurs after 30 min. Three repeated isotonic suspensions yelded all the activity thus obtainable (about 25% of total). Increasing the ionic strength of the suspension medium causes dramatic inactivation of the residual activity both in the extracted fraction and in the remaining one. It is confirmed that the bound activity is attached to chromatin.

Adenosine Monophosphate↗
PubMed1979

[Circadian rhythm of poly A polymerase in rat liver nuclei].

Isolated nuclei from the liver of rats maintained under daily scheduled conditions of light (12 hrs) and food (8 hrs) showed a peak of Mn2+-dependent poly (A) polymerase activity 6 hrs after the beginning of the feeding period, as shown by DNA dependent RNA polymerase B. In fasting animals the peak of poly (A) polymerase occurs at 18.00.

Animals↗
PubMed1979

[Effect of various methods of preparation of chromatin on the distribution of Mn2+-dependent poly-A-polymerase activity in subnuclear fractions of rat liver].

The distribution of Mn2+-dependent poly(A) polymerase activity between chromatin and nucleoplasmic fractions in rat liver nuclei strongly depends on the method followed for the chromatin preparation. Currently used methods containing high salt cause a loss in bound activity not accompanied by a correspondent increase in the "free" one.

Animals↗
PubMed1979

[Effect of administration of alpha-amanitine on Mn2+ - dependent poly-A-polymerase in rat liver nuclei].

Mn2+-dependent poly(A) polymerase activity tested in isolated rat liver nuclei is unchanged both in the absence and presence of exogenous poly(A) 30 min. after administration of a dose of alpha-amanitin that inhibits DNA-dependent RNA polymerase B. Longer times of treatment cause poly(A) polymerase to drop to 50% in the absence of poly(A) and to increase almost twice in its presence.

Amanitins↗
PubMed1979

[Concentrations of polyamines in maternal and umbilical-cord blood and in the amniotic fluid during normal human pregnancy and in feto-placental insufficiency].

Blood maternal polyamines during normal pregnancy exhibit an important augmentation around the 10th and the 34th-38th week, and a minor increase between the 20th-25th week of pregnancy. These peaks coincide with extremely important metabolic events in the feto-placental unit such as maximal growth rate in the placenta and fetus, respectively. The levels of polyamines measured from the 38th to 41th week in the blood of the umbilical cord are higher than in the blood of the mother. Putrescine, spermidine and spermine are not detectable when measured in the non-hydrolized amniotic fluid during normal pregnancy, instead a band with a lower Rf than spermine is present. In case of feto-placental insufficiency polyamine concentration in maternal blood are well below the normal values, from the 34th to 38th week of pregnancy. Such a behaviour appears for umbilical cord blood at the 38th and 39th week. Also the unknown polyamine of the amniotic fluid undergoes evident modification in feto-placental insufficiency. These results show that blood polyamines of the mother are probably of fetal origin, and that modified pattern of maternal polyamines may indicate an insufficient body growth of the fetus.

Adult↗
PubMed1979

[Serial evaluation of blood polyamines in children treated with growth hormone].

Blood polyamines were evaluated in normal children of various ages (from infancy to adolescence). Polyamines show a distinctive pattern: maximal values were observed during infancy; they decrease during childhood and again increase at puberty. After i.m. injection of Human Growth Hormone (HGH), polyamine concentrations increase significantly in the first 60 minutes. Polyamines increase more in patients previously untreated or treated intermittently with HGH than in patients under continuous treatment. The results suggest that in humans as well as in animals, polyamines could be involved in the growth processes and that the effect of HGH probably consists in a stimulation of polyamine synthesis.

Adolescent↗